Paternal obesity: how bad is it for sperm quality and progeny health?

Raad, Georges; Hazzouri, Mira; Bottini, Silvia; Trabucchi, Michèle; Azoury, Joseph; Grandjean, Valérie

doi:10.1186/s12610-017-0064-9

Cited by 54 publications

(36 citation statements)

References 148 publications

(141 reference statements)

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“…Even if obesity does not consistently reduce sperm counts or motility, it may still impact male fertility if sperm transmit damaged DNA or epigenetic alterations that reduce embryonic development or offspring health . Yet, once again, evidence for a link between male BMI and offspring developmental outcomes is mixed.…”

Section: Introductionmentioning

confidence: 99%

High‐fat diets reduce male reproductive success in animal models: A systematic review and meta‐analysis

Crean

Senior

2019

Obesity Reviews

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Sperm counts have shown a progressive decline across the world since the mid-1900s. Global rates of obesity have been climbing at a similarly alarming rate, suggesting that these two factors may be linked. However, studies examining the relationship between body mass index (BMI) and male fertility have produced conflicting results.These discrepancies among studies are commonly attributed to limitations that are inherent in human studies such as correlational data and confounding factors-limitations that are absent from animal studies. Hence, we conducted a systematic review and meta-analysis of animal studies that experimentally induced obesity with a high-fat diet and measured impacts on sperm traits and/or male fertility. Overall, we found strong, consistent evidence in animal studies that high-fat diets are detrimental for male fertility. Compared with controls, males fed a high-fat diet had smaller testes and sex accessory glands relative to body size, reduced semen quality, reduced mating success, and reduced fertilization success. This is the first time that experimental data of high-fat diet effects on male reproduction have been synthesized in a metaanalysis, and thus, our results provide novel insight to the complex question of how dietary-induced obesity affects male fertility. The strong negative effects detected in animal models suggest that the inconsistent results plaguing human studies are an artefact of limitations inherent in correlational studies rather than a true effect.

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Section: Introductionmentioning

confidence: 99%

High‐fat diets reduce male reproductive success in animal models: A systematic review and meta‐analysis

Crean

Senior

2019

Obesity Reviews

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“…Associations between maternal obesity, epigenetic alterations, and congenital malformations have also been proposed [ 23 , 24 ]. Finally, also considering the father's severe obesity, the role of the epigenetic paternal profile should not be excluded [ 25 ].…”

Section: Discussionmentioning

confidence: 99%

Type IV Laryngotracheoesophageal Cleft Associated with Type III Esophageal Atresia in 1p36 Deletions Containing the RERE Gene: Is There a Causal Role for the Genetic Alteration?

Pelizzo

Puglisi²,

Lapi³

et al. 2018

Case Reports in Pediatrics

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The causes of embryological developmental anomalies leading to laryngotracheoesophageal clefts (LTECs) are not known, but are proposed to be multifactorial, including genetic and environmental factors. Haploinsufficiency of the RERE gene might contribute to different phenotypes seen in individuals with 1p36 deletions. We describe a neonate of an obese mother, diagnosed with type IV LTEC and type III esophageal atresia (EA), in which a 1p36 deletion including the RERE gene was detected. On the second day of life, a right thoracotomy and extrapleural esophagus atresia repair were attempted. One week later, a right cervical approach was performed to separate the cervical esophagus from the trachea. Three months later, a thoracic termino-terminal anastomosis of the esophagus was performed. An anterior fundoplication was required at 8 months of age due to severe gastroesophageal reflux and failure to thrive. A causal role of 1p36 deletions including the RERE gene in the malformation is proposed. Moreover, additional parental factors must be considered. Future studies are mandatory to elucidate genomic and epigenomic susceptibility factors that underlie these congenital malformations. A multiteam approach is a crucial factor in the successful management of affected patients.

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“…It seems that the association between obesity and semen parameters remains controversial. Although male obesity is supported to be associated with reduced reproductive potential and sperm DNA damage, the long-term consequences of paternal health on offspring health have not been well-elucidated [16,49].…”

Section: Obesity and Male Infertility (Observational Studies)mentioning

confidence: 99%

“…Many pathogenetic mechanisms for this interplay have been proposed. With regard to male infertility, these include the aromatization of testosterone to estrogen in peripheral tissues, decreased sex hormone-binding globulin (SHBG) production in the liver [15,16], increased endorphin concentrations [leading to lower luteinizing hormone (LH) pulse and gonadotropin releasing hormone (GnRH) production] [17] and increased oxidative stress, which promotes sperm DNA damage [18]. With respect to female infertility, the underlying mechanisms include functional alterations of the hypothalamic-pituitary-gonadal (HPG) axis due to insulin resistance and relative hyperandrogenaemia [14], disordered secretion of gonadotrophins and hyperleptinaemia, leading to impaired folliculogenesis and ovulatory dysfunction [19][20][21][22].…”

Section: Introductionmentioning

confidence: 99%

Vitamin D and Obesity: Two Interacting Players in the Field of Infertility

et al. 2019

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Obesity plays an important role in human fertility in both genders. The same is true for vitamin D, for which accumulating evidence from observational human studies suggests a key role for both male and female fertility. In the latter case, however, robust data from relevant interventional studies are currently lacking. It is also not clear whether obesity and vitamin D deficiency, besides their independent effect on human infertility, act in synergy. Several pathogenetic mechanisms may be proposed as a linkage between vitamin D deficiency and obesity, with respect to infertility. In any case, the independent contribution of vitamin D deficiency in obese infertile states needs to be proven in interventional studies focusing on either vitamin D supplementation in obese or weight loss strategies in vitamin D-deficient infertile patients.

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Paternal obesity: how bad is it for sperm quality and progeny health?

Cited by 54 publications

References 148 publications

High‐fat diets reduce male reproductive success in animal models: A systematic review and meta‐analysis

High‐fat diets reduce male reproductive success in animal models: A systematic review and meta‐analysis

Type IV Laryngotracheoesophageal Cleft Associated with Type III Esophageal Atresia in 1p36 Deletions Containing the RERE Gene: Is There a Causal Role for the Genetic Alteration?

Vitamin D and Obesity: Two Interacting Players in the Field of Infertility

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